Starting my rat on GW 501516 tomorrow. this thread had caused me concern for his health but reading a study published in the diabetes journals.org has swayed me to begin research. A snippet below I found very interesting. Basically states there were no side effects from GW501516 besides one participant developing a rash after administration. Dosage appears to be capped at 10mgs. Good cholesterol remained unchanged, bad and total cholesterol was lowered as was triglyceride levels. participant weight and liver fat were also decreased while insulin sensitivity increased as was fat oxidation.
Full article:
Activation of Peroxisome Proliferator?Activated Receptor (PPAR)? Promotes Reversal of Multiple Metabolic Abnormalities, Reduces Oxidative Stress, and Increases Fatty Acid Oxidation in Moderately Obese Men
RESULTS
There were no significant differences between the three groups after randomization. Thus, age, blood pressure, total cholesterol, apoB, HDL cholesterol, and triglycerides were balanced between groups (
Table 1). There was no difference in baseline ALT and AST concentrations between the groups (
Table 1). Three of six subjects in the GW501516- and GW590735-treated groups fulfilled the The National Cholesterol Education Program Adult Treatment Panel III criteria for the metabolic syndrome (
39), whereas two of six fulfilled the criteria in the placebo group.
Tolerability.
There were no significant symptomatic side effects, and the results of liver (AST and ALT), hematology (blood cell counts), and renal function (creatinine) tests were unchanged in all groups. The concentration of γGT was unchanged in the placebo and GW590735 groups, but a 23% (
P < 0.05) lowering was seen in response to GW501516 treatment (
Table 2).
One subject developed a skin rash within 24 h after the first dose of GW590735, leading to withdrawal from the study. Treatment allocation for this patient remained concealed after this event, and a new subject was recruited to continue the study with the same blinded treatment allocation. Body weights did not change in placebo and GW590735-treated subjects, whereas subjects treated with GW501516 tended to lose weight (−1.7 ± 0.7 kg,
P = 0.05) over the 2-week treatment period.
Fasting plasma metabolic characteristics.
Total and LDL cholesterol were reduced by 20 and 23%, respectively (both
P < 0.05), accompanied by a 21% lowering of apoB (
P < 0.05) in subjects receiving GW501516 (
Table 2). HDL cholesterol was unchanged. Triglycerides were lowered by 31% (
P < 0.05). There was a very distinct lowering of fasting plasma NEFA (−40%,
P < 0.01). The lowering of NEFA was supported by significant lowering (−25%,
P < 0.05) of fasting plasma glycerol (data not shown). Treatment with GW590735 resulted in a similar reduction in fasting plasma triglycerides (−27%,
P < 0.05) but no change in NEFA (
Table 2) or glycerol (data not shown). LDL cholesterol did not change significantly, whereas a modest reduction in apoB (−13%,
P < 0.05) was observed with GW590735. HDL cholesterol tended to increase. Corresponding changes in lipids and lipoproteins in placebo-treated subjects were small and not statistically significant.
Fasting plasma insulin concentration was slightly reduced in response to GW501516 together with a small reduction in fasting plasma glucose (
P < 0.05). This led to a significantly improved insulin sensitivity, calculated as homeostasis model assessment of insulin resistance (
40), which was not seen in the GW590735 and placebo groups (
Table 2).
Liver fat.
There was no statistically significant difference in liver fat content between the groups at baseline. The GW501516-treated group exhibited a 20% reduction in liver fat that was statistically significant after adjustment for baseline fat content (
Fig. 1). Liver fat content in both GW590735-treated and placebo subjects tended to increase during the treatment period; neither of these changes were statistically significant.